کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10768864 | 1050816 | 2005 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A role of opening of mitochondrial ATP-sensitive potassium channels in the infarct size-limiting effect of ischemic preconditioning via activation of protein kinase C in the canine heart
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: A role of opening of mitochondrial ATP-sensitive potassium channels in the infarct size-limiting effect of ischemic preconditioning via activation of protein kinase C in the canine heart A role of opening of mitochondrial ATP-sensitive potassium channels in the infarct size-limiting effect of ischemic preconditioning via activation of protein kinase C in the canine heart](/preview/png/10768864.png)
چکیده انگلیسی
The opening of mitochondrial ATP-sensitive K+ (mitoKATP) channels triggers or mediates the infarct size (IS)-limiting effect of ischemic preconditioning (IP). Because ecto-5â²-nucleotidase related to IP is activated by PKC, we tested whether the opening of mitoKATP channels activates PKC and contributes to either activation of ecto-5â²-nucleotidase or IS-limiting effect. In dogs, IP procedure decreased IS and activated ecto-5â²-nucleotidase, both of which were mimicked by transient exposure to either cromakalim or diazoxide, and these effects were blunted by either GF109203X (a PKC inhibitor) or 5-hydroxydecanoate (a mitoKATP channel blocker), but not by HMR-1098 (a surface sarcolenmal KATP channel blocker). Either cromakalim or diazoxide activated both PKC and ecto-5â²-nucleotidase, which was blunted by either GF109203X or 5-hydroxydecanoate, but not by HMR-1098. We concluded that the opening of mitoKATP channels contributes to either activation of ecto-5â²-nucleotidase or the infarct size-limiting effect via activation of PKC in canine hearts.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 338, Issue 3, 23 December 2005, Pages 1460-1466
Journal: Biochemical and Biophysical Research Communications - Volume 338, Issue 3, 23 December 2005, Pages 1460-1466
نویسندگان
Osamu Tsukamoto, Hiroshi Asanuma, Jiyonng Kim, Tetsuo Minamino, Seiji Takashima, Akiko Ogai, Akio Hirata, Masashi Fujita, Yoshiro Shinozaki, Hidezo Mori, Hitonobu Tomoike, Masatsugu Hori, Masafumi Kitakaze,